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Maternal and offspring Mthfr genotypes interact in a mouse model to induce autism spectrum disorder-like behavior.
The data suggest that MTHFR deficiency decreases recovery after stroke by reducing neuronal and astrocyte viability.
data provide evidence for a similar cross-species response to high dose folic acid supplementation, of sperm DNA hypomethylation, and implicate MTHFR downregulation as a possible mechanism.
findings indicate that the loss of folate as a methyl donor is a modifier of allergic airway disease, and that epigenetic and expression changes correlate with this modification.
Ganglion cell loss and vasculopathy observed in Mthfr+/- and Cbs+/- mouse retinas may be milder than expected, not because of compensatory increases of enzymes in remethylation/transsulfuration pathways, but because downstream transsulfuration pathway products GSH, taurine, and H2S are maintained at robust levels.
In summary, high folate intake during pregnancy leads to pseudo-MTHFR deficiency, disturbed choline/methyl metabolism, embryonic growth delay and memory impairment in offspring. These findings highlight the unintended negative consequences of supplemental folic acid.
Study demonstrated that maternal MTHFR deficiency (i.e., in utero MTHFR deficiency) and early life exposure to vigabatrin separately and together alter the levels of proteins in the glutamatergic synapse
Mildly hyperhomocysteinemic Mthfr+/- mice demonstrate reduced ganglion cell function, thinner NFL, and mild vasculopathy by 24 weeks.
DNA methylation patterns in undifferentiated spermatogonia are relatively stable in culture over time under conditions of altered methionine and MTHFR levels.
Data from Mthfr knockout mice (in homozygous/heterozygous matings) suggest that maternal genotype contributes to sensitivity to arsenic as embryotoxin (i.e., genetic predisposition to fetal resorption/congenital malformation in arsenic poisoning).
our results support an interaction between mild neonatal stress, the MTHFR genotype and sex
expressed in placenta at highest level during early development
investigation of Mthfr regulation in an in vivo mouse model revealed temporal- and tissue-specific regulation that supports important roles for MTHFR in the developing embryo, and in postnatal brain and male reproductive tissues
A possible mechanism for the epigenetic involvement of Mthfr deficiency is proposed in the gender-dependent regulation of proteins associated with plasticity of the excitatory synapse.
These results showed that methylenetetrahydrofolate reductase deficiency impairs endothelial progenitor cell formation and increases endothelial progenitor cell senescence by endothelial nitric oxide synthase uncoupling and downregulation of SIRT1.
Variable presentation of MTHFR deficiency in different genetic backgrounds; plasma homocysteine is not a predictor of severity.
Newborn reflex development was slightly influenced by Mthfr +/- genotype and by the combination genotype and the neonatal vigabatrin (GVG) administration, in a sex-independent manner. Females presented attenuated anxiety due to Mthfr +/- genotype and GVG.
multiple transcription start sites and alternative splicing
reduces 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, the major carbon donor in the remethylation of homocysteine to methionine
Mthfr(+/-) genotype sensitizes mice to diet-induced hyperhomocysteinemia and hyperhomocysteinemia alters tissue methylation capacity and impairs endothelial function in cerebral microvessels.
MTHFR is critical for production of S-adenosyl-l-methionine (SAM), the principal methyl donor. A common mutation (1364T/T) of the cystathionine-gamma-lyase (CTH) gene affects the enzyme that converts cystathionine to cysteine in the transsulfuration pathway causing plasma elevation of total homocysteine (tHcy) or hyperhomocysteinemia-a strong and independent risk factor for cognitive loss and Alzheimer's disease
The heterozygosity for MTHFR (rs1801133, rs1801131) and FVII (rs6046) polymorphisms, that could determine genetic predisposition to thrombosis, is high in Turkish Cypriot population.
in patients with ischemic stroke, TT genotype is related to wind phlegm stasis syndrome, and CT genotype is related to Yin deficiency wind syndrome
High plasma homocysteine levels were linked to the MTHFR gene mutation in Northeast China. In addition, plasma homocysteine levels increased significantly with age with male's homocysteine levels higher than that of females.
The conventional use of large doses of folic acid (5 mg/day) has become obsolete. Regular doses of folic acid (100-200 mug) can be tolerated in the general population but should be abandoned in the presence of MTHFR mutations, as the biochemical/genetic background of the patient precludes a correct supply of 5-MTHF, the active compound
Assessment of the sufficiency of Moscow population with folic acid, depending on the combined effect of polymorphism of MTHFR and FTO genes.
Our data implied that common MTHFR polymorphisms of ectopic trophoblastic tissue are not associated with MTX failure in patients with tubal pregnancies. Additionally, serum beta-hCG concentration changes caused by MTX treatment and studied MTHFR polymorphisms are likely independent.
MTHFR C677T gene polymorphism may be a risk factor for metabolic syndrome in people in Hubei Province, China .
Is there a role for the MTHFR 677C>T and 1298A>C polymorphisms in methotrexate-induced liver toxicity?
MTHFR C677T polymorphism is not associated with diabetic retinopathy.
This study is the first to show associations between MTHFD1 1958G>A, RFC-1 80G>A, MTHFR 677C>T, and MTHFR 1298A>C polymorphisms and UPL and to compare the effects of maternal and fetal samples on unexplained pregnancy loss using mother-abortus matched samples of Korean origin.
Both CT genotype and T allele of MTHFR C677T gene polymorphism were found to pose significant decreased risk for cognitive impairment in apopulation based study from North India.
This study demonstrated maternal C677C MTHFR gene polymorphisms as a risk factor for ADHD.
MTHFR C677T polymorphism with smoking is associated with diabetic nephropathy in type 2 diabetes.
This meta-analysis showed that MTHFR C677T polymorphism was not significantly associated with alcohol dependence susceptibility compared to controls.
In a subgroup of Chinese hypertensive patients who had received 5-year antihypertensive therapy, increases in folate status were associated with higher reductions in PWV, and individuals with the CC genotype showed greatest PWV response to folic acid supplementation.
Our study suggested that the MTHFR C677T polymorphism may contribute to diabetic retinopathy development in multiethnic groups. Studies with larger sample sizes and wider spectrum of populations are warranted to verify this finding.
association between C677T polymorphism of MTHFR gene and congenital heart defects
This meta-analysis indicates that MTHFR C677T, A1298C, and MTRR A66G polymorphisms are the risk factors with susceptibility to male infertility in Asians.
Findings show no evidence for association of MTHFR 677C>T and 1298A>C variants with placental DNA methylation and pregnancy complications.
The protein encoded by this gene catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a co-substrate for homocysteine remethylation to methionine. Genetic variation in this gene influences susceptibility to occlusive vascular disease, neural tube defects, colon cancer and acute leukemia, and mutations in this gene are associated with methylenetetrahydrofolate reductase deficiency.
, 5,10-methylenetetrahydrofolate reductase (NADPH)
, methylenetetrahydrofolate reductase (NAD(P)H)
, methylenetetrahydrofolate reductase-like
, methylenetetrahydrofolate reductase